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1.
内皮素在肉鸡腹水综合征肺动脉高压中的病理学意义 总被引：2，自引：2，他引：0
肉鸡腹水综合征是当今世界各国肉鸡养殖业的一大难题 ,是造成肉仔鸡淘汰、死亡的重要原因之一。在许多国家 ,寒冷季节肉鸡腹水综合征造成的经济损失已经超过了传染病。对于我国肉鸡饲养业而言 ,大部分的肉鸡饲养集中于北方地区 ,每年饲养期有一半时间处于寒冷时期 ,因此肉鸡腹水综合征成为冬春季节危害最为严重的疾病之一。肉鸡腹水综合征的发病涉及环境、营养、遗传、饲养管理等多方面因素 ,目前普遍认为缺氧性肺动脉高压是肉鸡腹水综合征病理机制的中心环节 ,而肺血管收缩和肺血管结构重建为缺氧性肺动脉高压的特征。研究表明 ,肺及肺血管… 相似文献
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肉鸡腹水综合征 ,又称肺动脉高压综合征 ,是影响世界肉鸡饲养业的主要疾病之一。文章着重论述了肉鸡腹水综合征的病史、诱发因素、临床病理学特征以及诊断和治疗的最新研究进展 ,同时对其发病机理提出了三种假说。为进一步揭示其发病机理 ,更好地预防和治疗肉鸡腹水综合征提供了理论参考 相似文献
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肉鸡腹水综合征(Ascites syndrome,AS)是普遍发生于商品代肉仔鸡群的一种疾病,其特征是右心肥大、肝脏肿大及明显的腹腔积水。有学者根据肉鸡腹水综合征发病的病理变化和长期研究结果,提出肉鸡肺动脉高压假说,即发病因子→缺氧→肺动脉高压→右心肥大→右心室衰竭→肝脏淤血→腹水和死亡。其中肺动脉高压和右心肥大成为发病的关键环节。维拉帕米(Verapam il)是罂粟碱的衍生物,是一种钙离子内流阻滞剂(慢通道阻制剂),钙离子内流抑制使心肌细胞兴奋-收缩偶联中钙离子的利用降低,影响收缩蛋白的活动,心肌收缩减弱、心脏做功减少。试验旨在研… 相似文献
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雷小英 《兽药与饲料添加剂》1997,(6)
肉鸡腹水症是一种以腹腔蓄积大量液体为特征的疾病,又称心衰综合征、高海拔病或肉鸡腹水综合征。该病的发生有明显的季节性,一般多发于气候寒冷的冬季和早春季节,其病因比较复杂。目前普遍认为凡是能引起肉鸡肝脏、肺脏、肾脏和心脏损伤的因素均可诱发本病。1 发病诱因(1)饲养管理失误为了保暖而 相似文献
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肉用仔鸡腹水综合征（AS），又称肉鸡肺动脉高压综合征（PHS），是影响世界肉鸡养殖业的主要疾病之一。本病主要发生在冬春季节快速生长的４～７周龄肉鸡，以血液粘度升高、肺动脉高压、右心衰竭、肝脏淤血和腹腔积液为主症。目前认为，本病的发生与肉鸡生理机能本身、鸡舍环境低温、氨气、生长过快、饲料营养浓度太高、疫苗反应、呼吸系统疾病、曲霉菌病、遗传性过敏等因素有关。１肉仔鸡腹水综合征的发病原因肺动脉高压是AS发病机理的核心，引发的原因主要有：１．１缺氧１．１．１鸡舍通风不良，导致缺氧在冬季，鸡舍的通风换气受影响… 相似文献
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肉鸡肺动脉高压是以肺动脉压血管重构为特征的一种疾病,众多研究揭示肺血管重构是其中心环节之一。细胞内钙离子([Ca2+])浓度的升高是诱发并导致血管重构的重要机制,钙敏感受体(CaSR)在肺动脉平滑肌细胞内钙离子稳态失调及低氧性肺血管收缩和肺血管重构中起着重要的作用。应用免疫组化和Western blot方法研究了缺氧条件下CaSR在AA肉鸡和藏鸡肺动脉平滑肌组织中的表达情况,为肉鸡腹水综合征(PAH)的肺动脉重构提供新的证据。结果表明,肉鸡组有肺水肿发生,藏鸡组无肺水肿发生,缺氧条件下饲养的肉鸡肺动脉平滑肌CaSR表达明显高于藏鸡组(P0.05)。通过探讨CaSR在AA肉鸡和藏鸡肺动脉平滑肌组织中的表达情况,从新的角度阐明了肉鸡腹水综合征发生的分子机制。 相似文献
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张友新 《河南畜牧兽医(综合版)》2000,21(2):11-12
肉鸡腹水综合征是近年来流行在肉鸡饲养业中的一种生产性疾病。本病地理分布广泛 ,一年四季均可发生 ,尤以冬季多发。发病原因与环境因素、饲养管理因素、疾病因素、遗传因素等有关。发病机制主要是肺动脉高压和机体供氧不足造成的心、肺、肝的损害 ,导致机体血液循环障碍 ,部分血浆渗入腹腔造成腹水。本病目前尚未得到有效控制 ,针对本病发生的不同情况 ,主要采取综合防制措施。肉鸡腹水综合征常见于生长发育较快的４～１０周龄肉鸡群中。本病以明显的腹水 ,右心扩张 ,肺充血、水肿以及肝、肾等病变为主要特征。本病曾有过多种不同各称如营… 相似文献
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为了揭示肉鸡肺动脉高压的形成机理,为预防和治疗肉鸡腹水综合征提供理论依据,试验研究了两种钙颉颃剂硝苯地平和维拉帕米对肉鸡肺动脉高压和腹水肉鸡右心肥大指数的影响.结果表明:44日龄,硝苯地平组肺动脉压极明显低于低温组(P<0.01);28和36日龄,维拉帕米明显降低肺动脉压 (P<0.05);44日龄维拉帕米组肺动脉压极明显低于低温组(P<0.01).硝苯地平和维拉帕米可降低肉鸡腹水心脏指数.结果说明维拉帕米和硝苯地平降低了低温诱发的肺动脉高压和肉鸡腹水综合征的发生率,降低肉鸡腹水心脏指数,初步证实钙信号参与了肺动脉高压的形成. 相似文献
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肺动脉压升高是肉鸡肺动脉高压综合征(PHS)的重要发病机制。近年来研究表明一氧化氮(NO)在PHS发生发展中发挥着重要作用。本文论述了NO对肉鸡PHS发病过程的影响。一氧化氮合酶(NOS)和NO活性在PHS早期升高而后期下降。NO具有强大的扩张血管的作用,但在PHS过程中,NO合成相对不足,导致肺血管舒缩失衡,引起肺动脉压升高。肺血管重构是肉鸡肺动脉高压综合征的重要病理学变化特征,而NO可促进肺小动脉平滑肌细胞凋亡,在一定程度上抑制肺血管重构的形成。NO作为自由基对机体造成的损伤也是引起PHS的原因之一。在肉鸡日粮中补充NO前体物L-精氨酸可以增加内源性NO的生成,有助于降低PHS的发病率。 相似文献
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This article reviews recent nutritional approaches for counteracting the development of pulmonary hypertension syndrome (PHS; ascites) in broiler chickens especially when they are reared at high altitudes. High altitudes impose the sustained stress of hypobaric hypoxia, which reduces the availability of atmospheric oxygen to red blood cells passing through the lungs, thereby causing systemic arterial hypoxaemia (undersaturation of haemoglobin with oxygen), pulmonary arterial hypertension and PHS/ascites in susceptible broilers. Proper nutritional strategies are needed to reduce metabolic activity and prevent the development of ascites especially when modern broilers are reared in regions where the existing altitudes limit the availability of atmospheric oxygen. This article also addresses controversies with regard to broiler nutrition in relation to PHS. For example, the catabolism of protein from feed ingredients incurs increased oxygen consumption, suggesting that feeding reduced‐protein diets to broiler chickens may result in reduced PHS incidences. However, experimental and field data indicate that feeding reduced‐protein diets to broilers subjected to hypobaric hypoxia increases the development of PHS. Controversies on the nutrition of unsaturated fat in relation to PHS are also discussed. In conclusion, hypoxia, acidosis, vasoconstriction and enhanced metabolic rate are triggers of PHS. Feeding reduced‐protein diets might promote the susceptibility of broilers to PHS by decreased dietary intake of arginine, decreased uric acid production and increased lipogenesis. Feeding high‐protein diets, dietary arginine supplementation, partial substitution of sodium bicarbonate for sodium chloride, feeding low‐fat diets and effective feed restriction programmes can be considered as nutritional approaches to prevent PHS. 相似文献
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内皮素在肺动脉高压综合征肉鸡中的作用 总被引：1，自引：1，他引：1
通过急性试验确定内皮素（Endothelin，ET）对试验肉鸡肺动脉压的升压作用及其量效关系；在肉鸡快速生长期长时间给予ET，观察试验鸡发病率变化。结果表明：（1）在25ng／kg剂量静脉给予时，可引起肉鸡肺动脉压升高并达到与发病鸡相近的水平。（2）长期给予ET后，试验组30d发病率为6．7％，44d发病率13．3％，对照组发病率为0。同时，试验组红细胞压积（PCV）、腹水心脏指数（AHI）亦显著高于对照组。此结果表明，ET-1可通过缩血管效应引起肺动脉压升高，是致发肉鸡腹水综合征的一个重要因素。 相似文献
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《The Journal of Applied Poultry Research》2005,14(2):281-288
Ascites, also known as pulmonary hypertension syndrome (PHS), is a specific type of metabolic and cardiovascular disorder with a clear genetic component that affects fast-growing broiler chickens. In order to use genetic selection to reduce the incidence of PHS, a simple and easy to use indicator of PHS resistance or susceptibility in broiler breeders needs to be provided to geneticists. Electrocardiography is a noninvasive technology able to detect changes in heart function that have been associated with PHS susceptibility. Results from the present study demonstrated that broiler breeders having electrocardiographic parameters indicative of susceptibility or resistance to PHS produce progeny populations with high or low incidences of PHS. Furthermore, at the end of a 49-d grow-out period, progeny with the lowest PHS incidence also had significantly greater body weight and better feed conversion than progeny with the highest PHS incidence. These results indicated that electrocardiography could be successfully used to select for PHS resistance without detrimental effects on live performance. 相似文献
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Reduced erythrocyte deformability as a possible contributing factor to pulmonary hypertension and ascites in broiler chickens. 总被引：2，自引：0，他引：2
Deformability of erythrocytes and hematological parameters in white leghorn and broiler chickens were measured at age 7, 14, 21, 28, and 35 days. For deformability testing, a simple vertical apparatus containing a polycarbonate membrane with 5-microns pores was used. This technique assesses erythrocyte deformability by measuring the filtration time of an erythrocyte suspension through the pores. There was a significant difference in filtration time between the leghorns and broilers at all sampling times. These results indicate that reduced erythrocyte deformability in broilers may be one of the predisposing factors that increase resistance to blood flow and alter the rheology of blood in the microcirculation in the lung. Increased resistance to flow may result in pulmonary hypertension, heart failure, and ascites in broiler chickens. 相似文献
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Echocardiography was used to study cardiovascular structure and function during the development of pulmonary hypertension syndrome (PHS) in broiler chickens. Body weight-normalized right and left ventricular diameters at both end-diastole (RVDD, LVDD) and end-systole (RVDS, LVDS) were determined weekly in broilers reared under either normobaric (altitude, 96.7 m) or hypobaric conditions (simulated altitude, 2900 m) until 5 wk of age. Hypobaric-exposed broilers had larger RVDD at 3 and 4 wk of age and larger RVDS at 3, 4, and 5 wk of age. Hypobaric-exposed broilers also had larger LVDD at 2, 3, 4, and 5 wk of age and larger LVDS at 4 wk of age. Right (RVFS) and left ventricular fractional shortening (LVFS) were smaller in hypobaric- vs. normobaric-exposed broilers at 3, 4, and 5 wk of age and at 4 wk of age, respectively. Among hypobaric-exposed birds, PHS-positive (+) broilers had larger RVDD and RVDS than PHS-negative (-) broilers on week 3 and on weeks 1 and 3 after hypobaric exposure, respectively. PHS-positive (+) broilers also had smaller RVFS on week 1 after hypobaric exposure. Electrocardiographic and post-mortem data indicated that PHS+ broilers also developed right ventricular hypertrophy when compared with PHS-negative (-) broilers. These results are consistent with the hypothesis that PHS develops as a result of pulmonary hypertension and cardiac overload and suggest that PHS+ broilers have a greater and more persistent reaction to hypoxia than PHS- broilers. 相似文献
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Phonocardiography was evaluated as a noninvasive technique for diagnosis of cardiovascular adaptation and disease in broiler chickens. Heart sounds (HSs) were compared in a fast-growing (FG) commercial broiler line that is highly susceptible to chronic right heart failure resulting from pulmonary hypertension syndrome (PHS) and in a non-selected slow-growing (SG) broiler line that is resistant to PHS. HSs were analyzed in broilers reared in hypobaric hypoxia (HYP) and normobaric (CON) conditions. PHS was induced by a combination of embryonic hypoxia and HYP exposure. HSs were recorded with a microphone placed at the thoracic inlet of each chicken. Electrocardiograms were used to mark the sampling interval for the first, second, and total HS. Digitized HS signals were analyzed for peak frequency, mean peak frequency, and band width. Birds were examined for PHS lesions when 6 wk of age, at the end of each experiment. HSs were compared by line and treatment (Experiment 1) or by treatment and week (Experiment 2). In addition, HS frequencies were analyzed within the HYP treatment group for differences between birds with severe or no gross PHS lesions. HS frequencies generally decreased with age and were also lower in the FG than the SG line. Hypobaric exposure decreased all HS frequencies in the SG line and components of the first HSs in the FG line. The SG line did not develop gross lesions of PHS. In the FG line, significant differences in HS frequencies were observed between HYP and CON groups but not between PHS- and PHS+ broilers. Frequency changes described in humans with PHS were not observed. Further development to maximize the resolution of the HS waveforms and improved matching of the sampling interval to the electrical or hemodynamic output of the chicken heart may allow its use as a diagnostic tool for differentiating broilers with normal cardiac function or physiologic adaptation from those with cardiovascular disease. 相似文献
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Oxidative stress is involved in the development of pulmonary hypertension syndrome (PHS) in broilers. l-Carnitine has an antiperoxidative effect and supplemental l-carnitine has been revealed to increase broiler heart weight. The present study was conducted to evaluate the effect of an addition of 100 mg/kg l-carnitine to the basal diets on PHS mortality in cold-exposed broilers. Two-hundred and forty mixed-sex broilers were equally assigned to three groups. The control group was reared in normal temperatures throughout the experiment. Starting on day 14 continuing until the end of the experiment, the other two groups were subjected to a step-down temperature programme (by lowering the temperature 1-2 degrees C per day down to 12-14 degrees C) with or without l-carnitine added to the basal diets. Cold exposure increased the right/total ventricle ratio (RV/TV) and plasma malondialdehyde (MDA), reduced superoxide dismutase (SOD) and led to pulmonary vascular remodelling in birds without feeding additional l-carnitine. Supplemental l-carnitine reduced plasma MDA, increased SOD, inhibited remodelling and postponed the occurrence of PHS for 1 week in cold-exposed broilers; nevertheless, it did not significantly influence the cumulative PHS mortality (p > 0.05). On days 24 and 32, birds fed supplemental l-carnitine had lower RV/TV and higher total ventricle/body weight (p < 0.05) but unchanged right ventricle/body weight ratios (p > 0.05) compared to their cold-exposed counterparts, indicating an increase in left ventricle weight. However, from day 39 on, their RV/TV ratios were suddenly increased (p < 0.05). It was suggested that the l-carnitine-induced increase in left heart weight might partially account for the postponed occurrence of pulmonary hypertension in the early stage by elevating cardiac output, which might, in turn, lead to the resulting increase in pulmonary pressure. In view of its complex effects on cardiopulmonary haemodynamics, l-carnitine supplementation may be impractical for reducing PHS. 相似文献
19.
Effect of L-NAME on pulmonary arterial pressure,plasma nitric oxide and pulmonary hypertension syndrome morbidity in broilers 总被引：4，自引：0，他引：4
1. Experiments were conducted to evaluate the effect of a synthetic inhibitor of nitric oxide (NO) synthase (L-NAME) on pulmonary arterial pressure (PAP) and pulmonary hypertension syndrome (PHS) morbidity in broilers. 2. In Experiment 1, broilers were infused intravenously with L-NAME, and the mean pulmonary arterial pressure (mean PAP) and plasma NO were measured at 0, 1, 2 and 4 h after the start of infusion. The mean PAP increased and plasma NO was reduced at 1 to 2 h in broilers treated with L-NAME. 3. In Experiment 2, 180 Arbor Acres broilers were evenly divided into three groups: a control group (group C), and two groups exposed to low environmental temperatures and fed a 3, 3, 5-triiodothyronine (T3) supplemented diet alone (group A) or also including 100 ppm L-NAME (group B). 4. The PHS morbidity of group A was higher than for group C but lower than for group B. Plasma endothelin-1 was higher in broilers in groups A and B than in group C. Plasma NO was not significantly lower in broilers of group B when compared with those in group A. 5. The right/total ventricular weight ratio (RV/TV) and mean PAP were higher in groups A and B than in group C, and the RV/TV ratio increased one week earlier in group B than in group A. 6. These results suggest that L-NAME increases broiler PAP by inhibiting the endogenous synthesis of NO, leading to pulmonary hypertension, right ventricular hypertrophy and the increased morbidity of PHS in broilers. 相似文献